Abstract
Abstract Studies have been performed in a model teratologic system in which congenital malformations are produced in offspring by injecting sheep anti-rat kidney antiserum into pregnant rats on day 8 of gestation. To determine whether the antiserum produces its effects simply by combining with antigen, or whether direct participation of nonspecific mediators of immunologic damage is required, the antibody molecule was structurally altered by two methods: (1) a globulin fraction of the antiserum was reduced and alkylated to dissociate IgM antibody and destroy the complement-fixing ability of IgG antibody, and (2) a globulin fraction was digested with pepsin to destroy the Fc fragment of IgG. Both modified fractions retained the capacity to produce congenital malformations. This result suggests that complement and other nonspecific mediators are not involved in the immunologic damage which results in malformations in this system. The finding lends support to the proposition that this teratogenic antiserum acts by interfering sterically with normal yolk sac function during a critical period of fetal development.
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